I. Field of the Invention
This invention relates generally to a cardiac rhythm management device suitable for delivering stimulation pulses to a patient's heart and more particularly relates to a cardiac rhythm management device that utilizes a sensing protocol which avoids misidentification of artifacts and evoked potentials enhancing the ability of the device to sense intrinsic events.
II. Discussion of the Prior Art
Over the years, cardiac rhythm management devices have been utilized for supplanting some or all of an abnormal heart's natural pacing functions. These devices have remedied abnormalities including total or partial heart block, arrhythmias, congestive heart failure, congestive heart disorders and other various rhythm disturbances within the heart. Typically, the rhythm management device includes a power supply and pulse generator for generating electrical stimulus pulses delivered to a pre-selected area of the heart. An electrode lead arrangement (either uni-polar or bi-polar) positioned adjacent or within a pre-selected heart chamber is electrically coupled to the pulse generator for delivering stimulation pulses to the desired chamber. More recently, electrode lead arrangements have included multiple electrode leads positioned within a single chamber of the heart.
Regardless of the type of stimulation device employed to restore the heart's natural rhythm (i.e. defibrillators, Congestive Heart Failure (CHF) devices or other devices having logic and timing dependent on sensing of intrinsic heart events), each type operates to stimulate excitable heart tissue cells, which may or may not result in evoked response by the heart. Myocardial evoked response to stimulation or “capture” is a function of the positive and negative charges found in each myocardial cell within the heart. The selective permeability of each myocardial cell works to retain potassium and exclude sodium such that, when the cell is at rest, the concentration of sodium ions outside of the cell membrane are significantly greater than the concentration of sodium ions inside the cell membrane, while the concentration of potassium ions outside the cell membrane are significantly less than the concentration of potassium ions inside the cell membrane. When a stimulus is applied to the cell membrane, the selective permeability of the cell membrane is disturbed and no longer blocks the in-flow of sodium ions from outside the cell membrane. The in-flow of sodium ions at the stimulation site causes the adjacent portions of the cell membrane to lose its selective permeability, thereby causing a chain reaction across the cell membrane until the cell interior is flooded with sodium ions. This process, referred to as “depolarization”, causes the myocardial cell to have a net positive charge due to the in-flow of sodium ions and an out-flow of potassium ions. The success of a pacing stimulus in depolarizing or “capturing” the selected chamber of the heart is dependent upon whether the amplitude and/or duration of the stimulus as delivered to the myocardium exceeds a required threshold.
The effective delivery of stimulation pulses is further dependent upon the normal pacing cycle of the heart. The delivery of the stimulation pulse must be delivered at a proper time during the cardiac cycle or the stimulation pulse may not be effective, may not be as effective, or may be undesirable. The determination of the proper timing of the delivery of the stimulation pulse is further dependent upon proper detection of intrinsic activity in the heart. Polarization voltages and after potentials, which develop at the heart tissue electrode interface following the application of a stimulation pulse, affects the ability of the rhythm management device to accurately detect intrinsic activity. As pacemakers have evolved, the pacing modes and configurations have become more intricate and complex, generating an increasing array of polarization voltages and after potentials. Blanking or refractory periods, which may be considered as a means for avoiding unwanted sensing in the cardiac rhythm management devices, are frequently used to prevent artifacts and after potentials from being improperly detected as intrinsic events. Such blanking or refractory periods are typically initiated upon sensing an intrinsic activity or delivering a stimulation pulse and last until the end of all predictable artifacts and evoked potentials associated with the event. The blanking or refractory period, in effect, causes the pacing logic of the device to “ignore”, for example, detected intrinsic activity. Thus, the typical cardiac rhythm management device runs “blind” even if there is a period of time during this preset period for which no artifact or evoked potential is present and response to a detected intrinsic activity may be desirable.
For example, when pacing in the ventricles and sensing in the atrium, an atrial channel of a sensing circuit of the present day cardiac rhythm management devices may have to be refractory most of the time because of a long retrograde conduction time. Consequently, a P-wave resulting from intrinsic depolarization may easily fall into a refractory or blanking period, in which case the intrinsic atrial events will not be detected by the device. This reduces the effectiveness of the stimulation protocol of the device. U.S. Pat. No. 5,735,881 to Andre Routh et al. provides a method for increased sensing of intrinsic depolarizations by bifurcating the blanking period with an atrial sensing period. The Routh et al patent teaches the use of a fixed blanking period during the post ventricular atrial refractory period (PVARP) and a programmable blanking period to prevent the mischaracterization of a far field R-wave as an atrial depolarization event. However, the Routh et al patent does not teach or suggest a method for accounting for the complex polarization voltages and after potentials generated by multiple site pacing. Multiple site pacing may include at least one pacing/sensing site in an atrium and several pacing/sensing sites in one or more ventricles. Each intrinsic and each paced event in each of these sites may introduce one or more unwanted potentials in cardiac signals associated with the pacing/sensing sites. Each unwanted potential may have a relatively fixed temporal relationship with at least one intrinsic or paced event in one of the sites. Because whether such unwanted potentials will be present for an individual patient and how they are temporally related to any of the intrinsic and paced events are not necessarily known before device implantation, applying a programmable blanking period, as suggested by Routh et al., will require numerous blanking refractory periods. The number of such blanking or refractory periods will grow exponentially with the number of pacing/sensing sites in a multiple site pacing system, eventually to a point that requires a system size that cannot be accommodated by an implantable device and, moreover, this causes significant difficulties and potential for confusion to the physician programming the implantable device. What is, therefore, needed is one or more blanking or refractory periods that do not require excessive system resources and which are easy to program by a physician who observes the cardiac signals during or after a device implantation. The present invention meets these and other needs that will become apparent from a review of the description of the present invention.